4 Glomerulonephritis Principles Of Therapy

Glomerulonephritis

Principles of therapy

Current treatment of GN has two main objectives: control of inflammation and inhibition of fibrosis. Anti-inflammatory agents include intravenous or oralcorticosteroids, cyclophosphamide, azathioprine, mycophenolate mofetil, and fish-oil supplements containing omega-3 fatty acids. Drugs that reduce proteinuria will inhibit tubular injury and fibrosis[1]. These may include angiotensin-converting enzyme inhibitors (ACEi), angiotensin 2 receptor blockers (ARB), and perhaps statins and anti-oxidants. Specific treatments will be discussed in eachsection.

Acute glomerulonephritis

An adolescent with GN may present with signs and symptoms that require immediate intervention. One scenario is a presentation of renal insufficiency that worsensdaily, as evidence accumulates that the patient does not have PSAGN. Such patients may have rapidly progressive GN (RPGN) that is characterized pathologically by crescents forming from the cells ofBowman’s capsule. If the process progresses, the crescent will irreversibly destroy the glomerular tuft. ESRD may occur within weeks of the onset of this process. This process is a true emergency that requiresprompt referral to a nephrologist. Treatment with highdose intravenous methylprednisolone and, in some cases, plasmapheresis may halt the process [4–7]. Another scenario is the occurrence ofhypertensive encephalopathy or pulmonary edema at the onset of PSAGN. Adolescents who present with hypertension should be admitted to control the blood pressure and prevent these complications.

Rapidlyprogressive glomerulonephritis

RPGN may be diagnosed in the adolescent who presents with macroscopic hematuria and is found to have an elevated serum creatinine that continues to rise on a daily basis.Nonspecific symptoms such as fatigue and lethargy are common. Often the macroscopic hematuria persists until well after the initiation of treatment with intravenous methylprednisolone. Typically,...